Interactions Between Sleep and the Immune, Nervous and Endocrine Systems: A Narrative Review
Year: 2026
Type: review
Abstract: Background. Sleep is an elementary physiological process that is controlled by the circadian rhythm. It is crucial for maintaining homeostasis and proper functioning of many systems in the human body. Aim. The aim of this review is to summarize current knowledge on the impact of sleep deprivation on the immune, neurological, and endocrine systems. Material and methods. The narrative review of the literature was conducted using databases including PubMed. Studies were selected based on their clinical relevance. This article focuses on the latest observational studies, reviews and randomized trials. Results. In the nervous system sleep deprivation disrupts several brain functions, including cognitive performance, memory consolidation and neurodevelopment. Insufficient sleep is also associated with increased risk of neurological disorders, such as stroke and neurodegenerative diseases. Endocrine disturbances caused by the lack of adequate sleep include changes in secretion of many hormones, namely growth hormone, cortisol, melatonin, leptin and insulin. As a result, those changes lead to metabolic dysregulation, increased risk of obesity and type 2 diabetes. Sleep deprivation also impairs the immune function by altering leukocyte activity, reducing natural killer cell function, and increasing pro-inflammatory cytokine levels. Those shifts may contribute to the development of autoimmune disease and increase the susceptibility to infections. Conclusions. Sleep plays a crucial role in maintaining health and homeostasis. Its deprivation has many unfavorable effects on physiological pathways. Ensuring sufficient sleep duration and quality is essential for maintaining both, physical and mental health.
Source: Quality in Sport
Institution: Wroclaw Medical University
Language: English
Subfield: Experimental and Cognitive Psychology
Field: Psychology
Domain: Social Sciences
Open Access status: diamond
OpenAlex ID: W7166317779
